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smooth/antimykotikum
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Smooth-muscle rectal tumors: a therapeutic dilemma.
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Five cases of smooth-muscle rectal tumors seen in the Lexington, Kentucky, area over a 25-year period are reported. These unusual tumors cause symptoms similar to those of more common anorectal diseases, namely, painful defecation and rectal bleeding. Often these tumors are initially asymptomatic
[Airway smooth muscle responsiveness].
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Responsiveness of airway smooth muscle is influenced by various factors including autonomic nervous system, inflammatory cells and degrading enzymes. Hyperresponsiveness of airway smooth muscle may elucidated by functional abnormalities of inhibitory factors and abnormal production of potentiating
Tumors with smooth muscle differentiation.
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BACKGROUND
In the classification of tumors of soft tissue, modern schemes describe tumors by the normal adult tissue type the tumor resembles. Thus, tumors are described as smooth muscle tumors if the cells are differentiating towards smooth muscle. We may infer that in fact the tumor arose from
Airway smooth muscle: immunomodulatory cells?
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Evidence suggests that airway smooth muscle, the most important cell modulating bronchomotor tone, plays an important immunomodulatory role in the orchestration and perpetuation of airway inflammation. The signaling pathways that modulate leukocyte function may be disparate from those found in
Airway smooth muscle and asthma.
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The airway smooth muscle is the key determinant of airway narrowing in asthma but its function in the absence of disease is unknown. Evidence for an intrinsic abnormality in the muscle in asthma is only just emerging. The airway smooth muscle is not merely a contractile cell, but also one which
Ion channel gene therapy for smooth muscle disorders: relaxing smooth muscles to treat erectile dysfunction.
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The promise of gene therapy to treat diseases remains largely unfulfilled. Past setbacks and the complexity of the delivery systems used, in terms of both targeting the appropriate cells and inducing expression of products at therapeutic levels, thus far have prevented significant success for gene
TRP channels in airway smooth muscle as therapeutic targets.
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Cation channels are of fundamental importance in regulating the function of airway smooth cells especially bronchoconstriction in response to spasmogens, and are therefore key players in the pathogenesis of asthma. To date, the identity of these cation channels remains a mystery. However, the
Therapeutic interventions aimed at reducing airway smooth muscle growth.
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The airways of asthmatic subjects undergo complex changes which affect all compartments of the airway wall. The airway smooth muscle (ASM) is particularly affected and is increased in mass. Both hyperplasia and hypertrophy probably contribute to the altered mass of muscle which is a potential cause
Novel protein kinase targets in vascular smooth muscle therapeutics.
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Many signaling factors have been identified over the years that serve as mechanistic foundations for the pathogenesis and/or maintenance of cardiovascular disease (CVD). Of these, cyclic nucleotide-driven protein kinases in vascular smooth muscle (VSM) are of essential importance. Comprised
Therapeutic targets for overactive bladder other than smooth muscle.
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BACKGROUND
For a long time, our concepts of regulation of urinary bladder function in health and disease as well as of the target structures of therapeutics have focused on detrusor smooth muscle cells. However, other structures including urothelium, afferent nerves and bladder blood vessels may
Vascular Smooth Muscle as a Target for Novel Therapeutics.
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Cardiovascular disease is the principal cause of death in patients with type 2 diabetes (T2DM). Exposure of the vasculature to metabolic disturbances leaves a persistent imprint on vascular walls, and specifically on smooth muscle cells (SMC) that favours their dysfunction and potentially underlies
Airway smooth muscle cell as therapeutic target of inflammation.
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Airway inflammation is an outcome of complex interactions of multiple cell types in an inflammatory network. In recent years, it has become clear that a single target approach is unlikely to be effective for the treatment of inflammatory airway diseases such as asthma. This recognition suggests an
Mechanisms of Vascular Smooth Muscle Contraction and the Basis for Pharmacologic Treatment of Smooth Muscle Disorders.
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The smooth muscle cell directly drives the contraction of the vascular wall and hence regulates the size of the blood vessel lumen. We review here the current understanding of the molecular mechanisms by which agonists, therapeutics, and diseases regulate contractility of the vascular smooth muscle
Smooth muscle apoptosis and vascular remodeling.
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OBJECTIVE
The present review is to summarize recent advances in molecular mechanisms that regulate vascular smooth muscle cell apoptosis during vascular remodeling. In normal blood vessels apoptosis counteracts cell division, whereas apoptosis is especially crucial for regulating vascular remodeling
Calcium and vascular smooth muscle tone.
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Recent technologic advances have improved the monitoring of intracellular ionized calcium concentrations ([Ca2+]i) in living vascular smooth muscle cells. The changes in cytoplasmic ionized calcium concentrations ([Ca2+]) that occur during a contraction-relaxation cycle of vascular smooth muscle are
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